ArticleCellular & molecular biology letters2016
Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair.
Article in Cellular & molecular biology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Response gene to complement 32 promotes tumorigenesis by mediating DNA damage repair and inhibits CD8+ T cells infiltration in diffuse large B-cell lymphoma.Frontiers in immunology · 2025Article
- Serum RGC-32 in children with systemic lupus erythematosus.Scientific reports · 2023Article
- Pumping the Brakes on Pulmonary Fibrosis: A New Role for Regulator of Cell Cycle.American journal of respiratory cell and molecular biology · 2022Article
- Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- The Effect of 3'-Hydroxy-3,4,5,4'-Tetramethoxy -stilbene, the Metabolite of the Resveratrol Analogue DMU-212, on the Motility and Proliferation of Ovarian Cancer Cells.International journal of molecular sciences · 2020Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Renal proteomic analysis of RGC-32 knockout mice reveals the potential mechanism of RGC-32 in regulating cell cycle.American journal of translational research · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of this study was to evaluate the influence of RGC-32 (response gene to complement 32) on cell cycle progression in renal tubular epithelial cell injury.
methodsNRK-52E cells with overexpressed or silenced RGC-32 were constructed via transient transfection with RGC-32 expression plasmid and RGC-32 siRNA plasmid, and the cell cycle distribution was determined. The expression levels of fibrosis factors, including smooth muscle action (α-SMA), fibronectin (FN) and E-cadherin, were assessed in cells with silenced RGC-32.
resultsThe cells were injured via TNF-α treatment, and the injury was detectable by the enhanced expression of neutrophil gelatinase-associated lipocalin (NGAL). RGC-32 expression also increased significantly. The number of cells at G2/M phase increased dramatically in RGC-32 silenced cells, indicating that RGC-32 silencing induced G2/M arrest. In addition, after treatment with TNF-α, the NRK-52E cells with silenced RGC-32 showed significantly increased expression of α-SMA and FN, but decreased expression of E-cadherin.
conclusionsThe results of this study suggest that RGC-32 probably has an important impact on the repair process of renal tubular epithelial cells in vitro by regulating the G2/M phase checkpoint, cell fibrosis and cell adhesion. However, the exact mechanism needs to be further elucidated.
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